One of the leading causes of death in the United States is ventricular fibrillation, an uncoordinated movement of the individual cells in the heart which results in complete disruption of the circulation. The only known treatment for this fatal arrhythmia is electric countershock; however, the overall success rate is disappointingly low, only about 30 percent-50 percent in most clinical settings. Experimental studies have suggested that this low rate of success is due in part to immediate post-shock refibrillation which shows itself as a failure to defibrillate. Previous work in this laboratory has shown that this dysfunction is related to a shock induced prolonged depolarization of the myocardial cell membrane lasting several seconds to several minutes. This work suggested that the ionic mechanism which produces this prolonged depolarization differs from that producing activation and that it may result from a nonspecific redistribution of ions across the membrane during the shock. However the specific ionic mechanisms underlying this dysfunction and the factors which potentialte or ameliorate it are largely unknown. The goal of this research is to determine whether the prologed depolarization takes place due to a nonspecific redistribution of ions through microlesions in the cell membrane during the shock, to determine the size of the lesions, and the effect of biphasic waveforms to decrease them. This work will use intracellular microelectrode techniques and fluorescent microcinematography to examine the dysfunction which occurs in "adult-type" cultured myocardial cells during high intensity electric field stimulation. The results are expected to suggest specific modifications in countershock procedures and to yield insight into the processes through which myocardial cells respond to a discrete stress leading to membrane depolarization, in this case, the short high-intensity electric shock.